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Biomedical subjects

B H Bulkley

Publications and source records attributed to B H Bulkley.

At least 37 records · Page 2Linked to original sources
PubMed1984

Myocardial injury and induction of arrhythmia by direct current shock delivered via endocardial catheters in dogs.

Although electrical ablation of ventricular tachycardia via percutaneous catheters has been recently accomplished in human beings, little is known of its pathologic or arrhythmogenic effects. We studied 21 open-chest anesthetized dogs in which an endocardial electrode catheter was percutaneously introduced into the left ventricle. Direct current (DC) shock was delivered by a standard defibrillator through the distal electrode to a back paddle. Cross-sectional two-dimensional echocardiographic studies were performed in the plane of the catheter (confirmed by epicardial metal beads), and blood flow was determined by the microsphere technique before DC shock and when the animals were killed 2 to 8 days later. Of 11 dogs receiving a total of 100 to 400 J, only three survived 48 hr compared with nine of 10 receiving 50 J and all three control dogs. Holter monitoring demonstrated sustained ventricular tachycardia (VT) (greater than or equal to 30 sec) in all 11 dogs monitored (six received greater than or equal to 100 J), beginning within 5 hr of the DC shock; three control dogs had no VT. Two dogs that died suddenly while being monitored showed ventricular fibrillation. Histologic examination revealed hemorrhagic contraction band necrosis in the shock zone, a type of injury similar to that observed in reperfusion necrosis. Necrosis of the left ventricle was 0.5% to 5%. There was no significant difference in necrosis between dogs receiving 100 J or more and those receiving 50 J (2.5 vs 1.7 g; p greater than .10). Percent systolic thickening determined in eight equally divided regions around the left ventricle showed no difference between the shock zone, perishock zone, or remote normal zone in dogs receiving 50 J.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Whipple bacilli within the tunica media of pulmonary arteries.

In the lungs of two patients dying with Whipple's disease, we found Schiff-positive bacilli within the tunica media of many pulmonary arteries. Tissue was examined from all five lobes of the lungs in both cases. There were no pulmonary emboli and no alveolar lesions of Whipple's disease. Focal degeneration of the tunica media was conspicuous in areas where bacilli were present, and at some sites there was some overlying intimal proliferation. Little inflammatory response was present. All the bacilli within the tunica media were free as single organisms or small clumps, and there were none within macrophages. Macrophages containing bacilli were occasionally found within the adventitia of the pulmonary arteries. The possible role of these lesions in the pathogenesis of chronic pulmonary arterial disease merits consideration.

Humans↗
PubMed1984

Endocardial abnormalities in left ventricular aneurysms. A clinicopathologic study.

To correlate morphologic subgroups of left ventricular aneurysms with the major clinical manifestations (ventricular arrhythmias, congestive heart failure, and systemic emboli), we studied 73 patients with such aneurysms--34 at autopsy and 45 after surgical excision. Sixty-three patients had a history of congestive heart failure, 5 had systemic emboli, and 28 had recurrent ventricular tachycardia. Two types of endocardial abnormalities were noted: thick endocardial plaque composed of fibrous elastic tissue that contained little or no thrombus (type I, 30 patients); and aneurysms with little or no endocardial fibroelastosis (type II, 43 patients), some with layers of thrombus obliterating the aneurysmal cavity. Emboli only occurred in 5 patients with type II aneurysms who had mural thrombi. Recurrent ventricular tachycardia occurred in 20 patients with type I aneurysms but only in 8 with type II (p less than 0.001), showing a relation between endocardial fibroelastosis and ventricular tachycardia. Structural differences in ventricular aneurysms thus appear to have pathophysiologic significance. Our findings have implications for the mechanisms of ventricular tachycardia in postinfarction patients and for its prevention by endocardial resection.

Adult↗
PubMed1984

The mechanism of mannitol in reducing ischemic injury: hyperosmolarity or hydroxyl scavenger?

The effectiveness of postischemic reperfusion with mannitol has been well documented in previous studies. Mannitol, a hyperosmolar agent, is also an effective scavenger of the cytotoxic hydroxyl radical. If mannitol acts solely as a hyperosmolar agent, hyperosmolar reperfusion with its isomer, glucose, should be equally effective. To elucidate the beneficial effect of mannitol, 24 isolated rabbit heart preparations were subjected to 60 min of hypothermic (27 degrees C) cardioplegic arrest and normothermic reperfusion. There were three study groups with eight hearts in each. Group I hearts were reperfused with an unmodified isosmolar solution. Group II hearts were reperfused with a hyperosmolar (350 mOsm/liter) solution containing glucose, and group III hearts had hyperosmolar (350 mOsm/liter) reperfusion with mannitol. Left ventricular function (developed pressure and maximum positive dP/dt) was measured isovolumically before and after ischemia. Coronary flow was measured volumetrically during reperfusion, and myocardial edema formation was determined after 45 min of reperfusion. Reperfusion with mannitol resulted in significant improvement in recovery of developed pressure (77.3 +/- 2.8% of control vs 65.5 +/- 2.9% in group I and 62.6 +/- 2.2% in group II; p less than .05). Mannitol-treated hearts also had significantly greater coronary flow throughout the reperfusion period and significantly less marked myocardial edema formation compared with hearts treated with isosmolar and hyperosmolar glucose. These data confirm the particular usefulness of mannitol in improving postischemic ventricular function, maintaining coronary blood flow during early reflow, and reducing myocardial edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Pathophysiology of atherosclerotic heart disease.

Coronary atherosclerosis is the major health problem of the twentieth century. Although there has been a recent decrease in mortality from this condition in many Western countries, the incidence has remained the same, and coronary atherosclerosis continues to be the leading cause of death. Our understanding of the disease process has been steadily increasing; however, much still needs to be clarified. The clinical presentations of coronary artery disease are diverse and not clearly linked to the severity or extent of the disease. Patients with similar coronary lesions present variously with stable and unstable angina or myocardial infarction, and all too many have sudden death as the initial clinical presentation. Recently, much attention has focused on the initial events leading to the development of atherosclerotic plaques. Current concepts unite formerly opposed views on the roles of intimal injury, platelets, lipids, and monoclonal smooth muscle cell proliferation in initiating atherogenesis. Progress has been made in understanding the early structural and functional alterations caused by myocardial ischemia. This understanding is leading to the development of interventions such as intracoronary thrombolysis to prevent or limit permanent myocardial injury. Measures to prevent serious complications of ischemic heart disease such as infarct rupture, aneurysm formation, and ischemic cardiomyopathy are still needed.

Angina Pectoris↗
PubMed1983

Nontransmural versus transmural myocardial infarction. A morphologic study.

Although "nontransmural" and "transmural" are morphologic terms used widely to distinguish patients with myocardial infarction, controversy exists as to their meaning regarding clinical course. For this study, a transmural infarct was defined as one that involves essentially the full thickness of the ventricular wall, and nontransmural was defined as something less. The purpose of this study was to identify true morphologic nontransmural acute (less than 21 days old) infarcts at autopsy and compare them with transmural (full-thickness) infarcts in age-matched subjects, for clinical and pathologic similarities and differences. Among the autopsy subjects, comparing 35 nontransmural and 35 transmural infarcts, there was no significant difference with regard to subjects' race or sex, chest pain, arrhythmias, heart block, or cause of death; transmural myocardial infarctions did have a higher frequency of new Q waves (30 of 35 versus six of 35, p less than 0.001) and presented more often with increasing dyspnea. At autopsy, there were no significant differences regarding heart weight, location of infarcts, severity of coronary disease, age of acute infarct, or total size of infarct (18 percent of left ventricle for nontransmural versus 22 percent for transmural). There was, however, a significantly greater tendency for those with nontransmural infarct to have evidence of prior infarction at autopsy (27 of 35 versus 19 of 35, p less than 0.05). Acute coronary thrombi in the distribution of the infarct were significantly more common among transmural myocardial infarcts (32 of 35 versus 18 of 35, p less than 0.001). Morphologically, the nontransmural infarcts showed mural involvement ranging from 20 to 90 percent of the left ventricle, and histologically showed more contraction band (i.e., reflow) injury (57 percent with more than 30 percent contraction band necrosis) compared with transmural infarcts (32 percent with more than 30 percent contraction band necrosis) (p less than 0.05). Fatal nontransmural and transmural infarcts have major clinical and pathologic similarities, but differences in number of prior infarcts, type of necrosis, and occurrence of coronary thrombi suggest differing pathophysiology. The heterogeneity of both transmural and nontransmural infarcts likely accounts for existing differences among clinical studies regarding prognosis. Although this classification system has value in the clinical setting, that at times it represents an imprecise oversimplification of infarct type should be recognized in assessing individual patients.

Aged↗
PubMed1983

Salvaging ischemic myocardium after myocardial infarction.

Today's sophisticated diagnostic techniques make it possible to determine, virtually at the bedside, the site and size of an infarct and its effect on the patient's hemodynamic status. Thus, it is now possible to identify the patient who will benefit from aggressive therapy and to spare those who do not need or will not be helped by such treatment. Three phases of management are discussed.

Adrenergic beta-Antagonists↗
PubMed1983

Extensive myocardial fiber disarray in aortic and pulmonary atresia. Relevance to hypertrophic cardiomyopathy.

Myocardial fiber disarray is a distinctive histopathologic finding seen in asymmetric hypertrophic cardiomyopathy. We studied 14 hearts with aortic atresia and intact interventricular septum, six hearts with pulmonic atresia and intact interventricular septum, eight normal infant hearts matched for age of the study hearts, and one nonadult heart with hypertrophic cardiomyopathy and asymmetric hypertrophy and quantitatively analyzed tissue sections through both ventricles and the septum. Normal hearts had an average overall fiber disarray of 8.7% (range 3.8-17%) of the left ventricle including septum. Hearts with pulmonary atresia had an overall disarray of 70.4% (range 13-97%) of the entire right ventricle, and those with aortic atresia 62.1% (range 26-97%) of the left ventricle. The one infant heart with hypertrophic cardiomyopathy showed 15.5% disorder of the left ventricular free wall, 75% disorder of the septum and 47% overall myocardial fiber disarray. Thus, while quantitative criterion distinguished normal from abnormal hearts, they did not distinguish among the various pathologic states. Although extensive myocardial fiber disarray is not exclusive to, or pathognomonic of, hypertrophic cardiomyopathy, it is a useful finding taken in the context of the overall disease. The sensitivity and specificity of this isolated morphologic observation as an indication of hypertrophic cardiomyopathy may be misleading.

Aortic Valve↗
PubMed1983

Impaired function of salvaged myocardium: two-dimensional echocardiographic quantification of regional wall thickening in the open-chest dog.

This study was designed to examine the functional properties of myocardium subjected to acute coronary occlusion but surviving the ischemic insult. Ten conscious mongrel dogs underwent mild-circumflex coronary occlusion and were treated for 6 hours with prostacyclin, 540 ng/kg/min, and ibuprofen, 110 micrograms/kg/min, or dipyridamole (7-9.7 micrograms/kg/min). At 7 days, each dog was anesthetized, the chest was opened, and cross-sectional two-dimensional echocardiograms were obtained through the middle of the occluded vascular bed. A computer-aided contouring system was used to assess percent systolic thickening in 16 equally spaced segments around the left ventricle. Metal markers sewn to the epicardium permitted precise regional correlation of histology, percent systolic thickening, and flow, as measured by radioactive microspheres. Necrosis was minimal, averaging only 2.2 +/- 0.8% (+/- SEM) of the left ventricular ring corresponding to the echocardiographic cross section. Percent systolic thickening was 28.6 +/- 4.7 in the nonischemic anterior wall, but was reduced to -4.5 +/- 3.1 in the occluded bed (p less than 0.01). In individual echo segments, percent systolic thickening correlated with local flow (r = 0.69, p less than 0.001), but was still depressed even when flow was normal. In six segments within the occluded bed that had normal histology and flow, percent systolic thickening was 52% less than that in the nonischemic region (p less than 0.02). Thus, coronary artery occlusion combined with drug treatment results in myocardium that, although histologically normal and supplied by normal myocardial blood flow, remains functionally abnormal 7 days after occlusion.

Animals↗
PubMed1983

Comparison of early thallium-201 scintigraphy and gated blood pool imaging for predicting mortality in patients with acute myocardial infarction.

The extent of abnormality in early thallium-201 and gated cardiac blood pool scintigrams has been reported to be useful for predicting mortality in patients with acute myocardial infarction (AMI). To compare the two techniques, 91 patients admitted consecutively with evident or strongly suspected AMI underwent both imaging studies within 15 hours of the onset of symptoms. Patients with pulmonary edema or shock were excluded. AMI developed in 84% of patients, and 6-month mortality for the entire group was 16%. A thallium defect score of 7.0 or greater (corresponding to at least a moderate reduction of activity involving 40% of the left ventricular circumference) identified a subgroup of 14 patients with 64% 6-month mortality rate. Similarly, a left ventricular ejection fraction of 35% or less identified a high-risk subgroup of 10 patients with a 6-month mortality of 60%. Mortality in the remaining patients was 8% for thallium score less than 7 and 11% for ejection fraction greater than 35%. The mortality rate was highest among patients who had concordant high-risk scintigrams (five of six, 83%), lowest in those with concordant low-risk studies (five of 64, 8%) and intermediate in those with discordant results (four of 11, 36%). Of a number of clinical variables, only the appearance of Q waves, peak creatine kinase greater than 1000 IU/I, and history of infarction were significantly associated with mortality. High-risk thallium or blood pool scintigraphic results were significantly more predictive and a thallium score of 7 or greater was more sensitive for detecting nonsurvivors than ejection fraction 35% or less at a similar level of specificity. Stepwise multiple logistic analysis showed that the thallium score was the best predictor of mortality, but that appearance of Q waves and ejection fraction were additive. Using these three variables, 11 patients were calculated to have a 50% or greater chance of dying and eight (73%) actually died, compared with six of 70 (9%) with a calculated chance of death of less than 50%. These results in a prospectively identified and consecutive group of patients support the value of early thallium and blood pool scintigraphy for separating high- and low-risk subgroups of hemodynamically stable infarct patients.

Adult↗
PubMed1983

Differences in Thallium-201 uptake in reperfused and nonreperfused myocardial infarction.

The respective importance of flow and cellular viability in determining initial myocardial thallium uptake was studied in reperfused and nonreperfused experimental myocardial infarction. Open-chest dogs were subjected to permanent coronary artery occlusion of 70-minute (n = 3) or 5-hour duration (n = 5), or to a 3-hour temporary occlusion followed by reflow (n = 14). Thallium uptake 10 minutes after intravenous injection was compared directly with radioactive microspheres in myocardial samples from excised hearts. Triphenyl tetrazolium chloride staining was used to differentiate necrotic and viable samples with confirmation by electron microscopy. In nonreperfused infarcts, thallium uptake occurred despite necrosis, and a close correlation was found between thallium uptake and regional myocardial blood flow. In reperfused infarcts, thallium uptake again occurred, but was reduced relative to flow in necrotic myocardium and, to a lesser extent, in reperfused viable areas. However, because of the high levels of reflow, actual thallium uptake was often more than 50% of normal in reperfused necrotic regions. This study demonstrates that the presence of thallium uptake is an unreliable indicator of myocardial injury and that reperfused necrotic tissue may have remarkably high levels of thallium uptake.

Animals↗
PubMed1983

A randomized clinical trial of intravenous nitroglycerin in patients with acute myocardial infarction: benefits of early treatment.

A prospective randomized clinical trial of intravenous nitroglycerin administered for 48 hours following acute infarction was undertaken to determine whether clinical improvement and/or preservation of ischemic myocardium could be demonstrated. One hundred four patients were randomized to receive either nitroglycerin or placebo infusion. Nitroglycerin infusion was titrated to lower mean arterial pressure 10% using non-invasive monitoring. Early nitroglycerin treatment, defined as treatment initiated less than 10 hours after symptom onset, resulted in a lower incidence of new congestive heart failure, myocardial infarct extension, and/or early death from pump failure (15%) compared to late nitroglycerin treatment (50%, p = 0.008) or early placebo treatment (48%, p = 0.01). Improvement in ejection fraction of greater than or equal to 10% was demonstrated in 7 of 20 (35%) early nitroglycerin treated patients compared to 6, 11 and 0% of patients in the three other subgroups, respectively (p = 0.004). Similarly, thallium-201 perfusion scintigrams showed a greater than 75% improvement in defect score in 23 (48%) patients receiving nitroglycerin within 10 hours compared to 14%, 33% and 0% respectively, in the remaining subgroups (p = 0.035). However, before routine administration of nitroglycerin can be recommended for all patients with acute infarction, larger clinical trials will be required.

Clinical Trials as Topic↗
PubMed1983

Improved myocardial preservation during global ischemia by continuous retrograde coronary sinus perfusion.

To investigate whether retrograde continuous low-pressure perfusion of the coronary sinus could deliver cardioplegic solutions with oxygen and substrate beyond stenoses and result in improved myocardial preservation, we subjected 41 canine hearts to 90 minutes of ischemia with an occlusion on the circumflex coronary artery. There were four groups: Group I, antegrade (aortic root) crystalloid cardioplegia every 30 minutes during ischemia; Group II, antegrade plus topical cooling; Group III, continuous retrograde perfusion; Group IV, same as Group III, with an oxygenated perfluorocarbon. All solutions had a PO2 of 400 to 500 mm Hg. Intramyocardial oxygen and carbon dioxide tensions (PO2 and PCO2) and mean myocardial temperatures were monitored during ischemia, and left ventricular (LV) function was assessed before ischemia and after reperfusion. After global ischemia, the circumflex occlusion was released and the hearts reperfused. Following 60 minutes of reperfusion, isovolumic developed pressure returned to 36% +/- 4% and 41% +/- 5% of preischemic levels, respectively, in Groups I and II. By contrast, Groups III and IV (retrograde perfusion) had a significantly greater percent of recovery (78% +/- 5% and 73% +/- 5%). Circumflex area intramyocardial PO2 fell 20 and 25 mm Hg below preischemic levels in Groups I and II during ischemia, whereas in Group III, intramyocardial PO2 in the circumflex region remained near preischemic levels, and in Group IV, it rose 19 mm Hg. Mean myocardial temperature during ischemia in the circumflex area was significantly higher in Group I than in Groups II, III, and IV. Peak intramyocardial PCO2 in the circumflex region was significantly less in the retrogradely perfused hearts. Retrograde coronary sinus perfusion resulted in significant improvement in recovery of LV function, uniform myocardial cooling, normal intramyocardial PO2, and less intramyocardial PCO2 accumulation, despite the presence of a total circumflex coronary artery occlusion.

Animals↗
PubMed1983

Enhanced myocardial protection with verapamil prior to postischemic reflow.

Reperfusion of the heart after induced myocardial ischemia may be associated with severe myocardial damage, characterized by massive calcium influx and accumulation in the heart cells. The present study was undertaken to investigate whether verapamil, a slow channel calcium blocker, administered prior to reperfusion, might reduce this reflow injury without causing depression of heart function. Thirty-two isolated, perfused rabbit hearts were subjected either to 45 minutes of normothermic or 150 minutes of hypothermic global ischemia. Half of the heart in each group received verapaMil immediately prior to reperfusion, while the remaining hearts received no verapamil. Following ischemia and 60 minutes of reperfusion, left ventricular (LV) contractivity was superior in both groups of verapamil-treated hearts, compared to control hearts (LV developed pressure [DP] in normothermic hearts 63 +/- 6% of preischemic DP for verapamil-treated hearts versus 46 +/- 6% of preischemic DP for control hearts; in the hypothermic group, 65 +/- 8% of preischemic DP for verapamil-treated hearts versus 33 +/- 10% DP for control hearts). Postischemic LV compliance also was significantly improved in the verapamil-treated hearts through the period of reperfusion, compared to control hearts. No differences were noted in coronary flow, myocardial water content, or the onset of electromechanical activity between the verapamil and control hearts, but there was significantly improved ultrastructural preservation in both verapamil groups. These data demonstrate that verapamil, when administered just prior to reperfusion, results in improved recovery of myocardial function and excellent cellular preservation, presumably for reducing calcium influx into myocardial cells.

Animals↗